Evidence map›Paper›PMID 31061124›Full record

ArticleProceedings of the National Academy of Sciences of the United States of America2019

Wnt canonical pathway activates macropinocytosis and lysosomal degradation of extracellular proteins.

Nydia Tejeda-Muñoz, Lauren V Albrecht, Maggie H Bui, Edward M De Robertis

Open access · bronzeAbstract read
In one paragraph

Article in Proceedings of the National Academy of Sciences of the United States of America, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 68 papers.

0numbers the graph read from it
0cells of the map it votes in
68citing papers in PubMed
5.0field-weighted citation impact, top 4% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

68 citing papers in PubMed, 110 citations in OpenAlex.

  1. Article
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  5. Article
  6. Article
  7. Review
  8. Article
  9. Article
  10. Article
  11. Article
  12. Article
  13. Wnt signalosomes: What we know that we do not know.BioEssays : news and reviews in molecular, cellular and developmental biology · 2025
    Review
  14. Review
  15. Article
  16. Review
  17. Article
  18. Novel selective inhibitors of macropinocytosis-dependent growth in pancreatic ductal carcinoma.Biomedicine & pharmacotherapy = Biomedecine & pharmacotherapie · 2024
    Article
  19. Article
  20. Cellular Regulation of Macropinocytosis.International journal of molecular sciences · 2024
    Review

8 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

4 authors at 2 institutions in 1 country.

Nydia Tejeda-MuñozHoward Hughes Medical Institute, University of California, Los Angeles, CA 90095-1662.
Lauren V AlbrechtHoward Hughes Medical Institute, University of California, Los Angeles, CA 90095-1662.
Maggie H BuiHoward Hughes Medical Institute, University of California, Los Angeles, CA 90095-1662.
Edward M De RobertisHoward Hughes Medical Institute, University of California, Los Angeles, CA 90095-1662; ederobertis@mednet.ucla.edu.
Howard Hughes Medical Institute · USUniversity of California, Los Angeles · US

Funding

UCLA Clinical and Translational Science InstituteUL1TR000124 · NCATS · UNIVERSITY OF CALIFORNIA LOS ANGELES · PI DUBINETT, STEVEN M. · 2012 to 2015
$57.0M
Wnt Signaling and Endosomal Trafficking as Regulators of Cellular Protein DegradationF32GM123622 · NIGMS · UNIVERSITY OF CALIFORNIA LOS ANGELES · PI ALBRECHT, LAUREN VERONICA · 2017 to 2019
$118k
Howard Hughes Medical InstituteNCATS NIH HHS UL1 TR000124NIGMS NIH HHS F32 GM123622
6 · The paper itself

Abstract

Canonical Wnt signaling is emerging as a major regulator of endocytosis. Wnt treatment markedly increased the endocytosis and degradation in lysosomes of BSA. In this study, we report that in addition to receptor-mediated endocytosis, Wnt also triggers the intake of large amounts of extracellular fluid by macropinocytosis, a nonreceptor-mediated actin-driven process. Macropinocytosis induction is rapid and independent of protein synthesis. In the presence of Wnt, large amounts of nutrient-rich packages such as proteins and glycoproteins were channeled into lysosomes after fusing with smaller receptor-mediated vesicles containing glycogen synthase kinase 3 (GSK3) and protein arginine ethyltransferase 1 (PRMT1), an enzyme required for canonical Wnt signaling. Addition of Wnt3a, as well as overexpression of Disheveled (Dvl), Frizzled (Fz8), or dominant-negative Axin induced endocytosis. Depletion of the tumor suppressors adenomatous polyposis coli (APC) or Axin dramatically increased macropinocytosis, defined by incorporation of the high molecular weight marker tetramethylrhodamine (TMR)-dextran and its blockage by the Na

Indexed as

AnimalsAxin Proteinbeta CateninCell LineCell Line, TumorEndocytosisGlycogen Synthase Kinase 3GlycoproteinsHeLa CellsHumansLysosomesMiceNeoplasmsNIH 3T3 CellsPinocytosisProtein-Arginine N-MethyltransferasesAxin Proteinbeta CateninGlycogen Synthase Kinase 3GlycoproteinsProtein-Arginine N-MethyltransferasesTrans-ActivatorsWnt Proteinsadenomatous polyposis coliarginine methylationESCRTmacropinocytosisWnt-STOP

Identifiers

PMID31061124
PMCPMC6534993
OpenAlexW2944232267

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.